Marc-Étienne HuotPh.D.

Dr. Marc-Étienne Huot holds a PhD in Cellular and Molecular Biology from Laval University. His laboratory, established at the CHU Research Center of Québec – at l’Hôtel-Dieu de Québec, studies the role of RNA-binding proteins in the various processes leading to the formation of metastases.

Dr. Huot’s laboratory is studying the mechanisms by which RNA-binding proteins regulate metastatic dissemination (Thematic 1), as well as cellular metabolism during tumor progression (Thematic 2).

Thematic 1 – Role of RNA-binding proteins in the regulation of tumor progression and metastasis formation. The involvement of mRNA regulation in tumor progression is often overlooked. Dr. Huot’s research attempts to overcome this omission by determining how RNA-binding proteins can regulate the spread of cancer cells, a complex process that allows them to leave the primary tumor to colonize and form secondary tumors (metastases) in distant tissues. Indeed, his results indicate that RNA-binding proteins (notably Sam68) can regulate several mechanisms essential to the formation of metastases, such as cell migration and adhesion. The hypothesis is that deregulation of RNA-binding protein activity affects the ability of metastatic cells to target the microenvironment of specific tissues. The results of his work will offer new therapeutic strategies to block tumor progression and thus prevent the formation of metastases.

Thematic 2 – Identification of non-canonical mTOR regulatory pathways in the control of cellular metabolism and tumor progression. Maintaining cell integrity requires close control of the cellular metabolism. Our second research theme concerns the regulation of mTOR, a central protein of cellular metabolism. In this theme, Dr. Huot is studying two new regulatory mechanisms affecting the mTOR protein. Part of his research attempts to elucidate how RNA-binding proteins associate with specific sequences present in mTOR mRNA to regulate splicing, stability, and activity. The second part concerns a mechanism that deregulates normal metabolic functions. This deregulation is caused by mutations frequently found in low-grade brain tumors, which would promote tumor progression by promoting the proliferation and survival of cancer cells. These results will make it possible to understand these new modes of regulation of cell metabolism that are usually deregulated in treatment-refractory cancers.